Background: Cardiovascular diseases (CVDs) are the leading cause of death worldwide. Within CVDs, cerebrovascular diseases (CeVDs) share risk factors with both stroke and dementia. Neuropathological lesions such as lacunar infarcts, hyaline arteriolosclerosis, and cerebral amyloid angiopathy are recognized contributors to cognitive decline. Yet, little is known about how the composition of carotid atherosclerotic plaques relates to these brain pathologies. This autopsy-based study investigates associations between carotid plaque components and cerebrovascular lesions relevant to dementia. Methods: We used data from the Biobank for Aging Studies at the University of São Paulo Medical School, with participants who were 50 or older at death, with a post-mortem interval under 24 hours, and an informant who had at least weekly contact with the individual, were eligible (n = 566). Carotid plaques were assessed histologically and quantified using the Atherosclerotic Plaque Analyzer software. Neuropathological evaluation followed internationally accepted protocols. Associations between plaque features and cerebrovascular lesions were tested using multivariable logistic regression models adjusted for sociodemographic and clinical variables. Results: Higher arterial obstruction (OR = 1.20, 95% CI 1.11–1.29) and IMT (OR = 1.08, 95% CI 1.01–1.15) were associated with increased LI risk. Similarly, HA was linked to greater stenosis (OR = 1.08, 95% CI 1.04–1.13), IMT (OR = 1.05, 95% CI 1.01–1.09), and plaque fibrosis. CAA showed no association but was related to necrosis in common carotid/bifurcation plaques (OR = 1.41, 95% CI 1.10–1.81) and lipid core in internal carotid segments (OR = 1.08, 95% CI 1.01–1.16). Stratified analyses revealed stronger associations in proximal carotid segments, suggesting location-dependent effects. Smooth muscle cell presence was protective against LI and HA, while plaque instability (necrosis, hemorrhage, or thrombus) increased HA risk. Conclusion: These findings demonstrate that carotid plaque composition and stenosis independently predict cerebrovascular injury, particularly LI and HA. This study provides a pathological association between atherosclerosis and cerebrovascular lesions, supporting targeted investigations to mitigate cognitive decline in aging populations.

Machine learning models for carotid artery plaque detection: A systematic review of ultrasound-based diagnostic performance.

Intraluminal drug coated devices, such as paclitaxel (PTX)-coated balloons, are commonly used to treat arterial occlusive diseases caused by atherosclerosis. However, their efficacy is limited by drug loss, poor drug retention, insufficient penetration and high costs. Nanoparticles with molecular targeting capabilities offer a promising solution to these challenges. Collagen hybridizing peptide (CHP) specifically binds to degraded collagen in atherosclerotic plaques, enabling precise molecular imaging and targeted therapy. In this study, we demonstrated that collagen degradation was significantly elevated in atherosclerotic plaques and could be effectively identified by CHP in both atherosclerosis patients and mice models. Using the emerging copper-free click chemistry reaction, we functionalized the widely used albumin-based indocyanine green nanoparticles and albumin-bound paclitaxel nanoparticles with CHP, developing a targeted nanoplatform for molecular imaging and therapy. In vivo photoacoustic (PA) imaging and ex vivo fluorescence (FL) imaging revealed significantly enhanced PA and FL signals in carotid artery and aorta plaques with CHP functionalized nanoparticles engaging. Furthermore, therapeutic evaluations showed that CHP significantly improved the plaque-targeting capability of albumin-bound paclitaxel nanoparticles, thereby enhancing their therapeutic efficacy against atherosclerotic plaques. These findings highlighted CHP-functionalized albumin nanoparticles as a promising strategy for precise and effective atherosclerosis molecular imaging and treatment.Graphical Albumin nanoparticles functionalized with CHP by copper-free click chemistry reaction, enhancing the imaging ability and therapeutic efficacy for atherosclerosis by elevated plaque targeting capability.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12951-025-03721-3.

Association between inflammatory cytokines and carotid plaque in young and middle-aged adults

This study aimed to develop and validate an effective nomogram combining clinical biomarkers and carotid plaque's superb microvascular imaging (SMI) features for predicting acute ischemic stroke. In this study, 326 patients with carotid plaque were enrolled, and all patients were divided into two datasets for training and validation. We constructed an integrated nomogram combining clinical and ultrasound characteristics of carotid plaque using LASSO regression and multivariable logistic regression to predict acute ischemic stroke. LASSO regression combined with multivariate logistic regression indicated that smoking index, stroke duration, diabetes duration, monocytes/lymphocyte ratio, the surface condition and SMI neovascularization level of plaque were independently related to acute ischemic stroke. The area under the curve for the nomogram to predict AIS was 0.839 (95% CI,0.789-0.888) in the training cohort, 0.785 (95% CI, 0.669-0.901) in the validation cohort. Our proposed acute ischemic stroke nomogram shows favorable predictive value to patients with carotid artery plaques and has positive clinical significance in individualized scientific management.

BackgroundCarotid plaque and fatty liver disease, as important target organ damages of metabolic disorders, have undergone a steady increase in prevalence. Cholesterol, high-density lipoprotein, and glucose index (CHG), triglyceride–glucose index (TYG), and atherogenic index of plasma (AIP) are tools for assessing metabolic abnormalities. This research aimed to evaluate the potential of three indicators in predicting carotid plaque and fatty liver.MethodsThis study is based on longitudinal health examination data from workers at Ansteel Group in China in 2019. The follow-up period was five years, with the outcomes being the occurrence of carotid plaque or fatty liver events. Multivariate Cox regression analysis was used to examine the relationship between CHG, TYG, and AIP with the outcomes of carotid artery plaque and fatty liver. We used restricted cubic spline (RCS) curves to analyze the dose-response relationship between the three indices and the outcomes. We employed receiver operating characteristic (ROC) curves to evaluate the predictive ability of these indices. Finally, we also conducted subgroup analyses.ResultsCarotid plaque events developed in 659 workers (18.40%), and fatty liver in 375 workers (10.47%) during the follow-up period. Cox analysis revealed that the three indices were correlated with carotid plaque (Q3 vs Q1, CHG: HR 2.13, P < 0.001; TYG: HR 1.20, P = 0.006; AIP: HR 1.95, P < 0.001) and fatty liver (Q3 vs Q1, CHG: HR 2.46, P < 0.001; TYG: HR 1.75, P < 0.001; AIP: HR 3.47, P < 0.001). RCS indicated that the three indices were linearly related to carotid plaque and nonlinearly (inverted L-shaped) related to fatty liver. ROC curve analysis revealed that CHG had a stronger predictive ability for carotid plaque outcomes, while TYG had a stronger predictive ability for fatty liver. Subgroup analysis results showed that gender and BMI interacted with the three indicators in relation to outcomes.ConclusionsOur research found that CHG, TYG, and AIP were positively correlated with carotid plaque and fatty liver. Moreover, CHG demonstrated superior predictive ability for carotid plaque outcomes, whereas TYG demonstrated better performance for fatty liver outcomes.

ObjectiveThis study aims to investigate the correlation between the triglyceride-glucose (TyG) index and intraplaque neovascularization (IPN), evaluate the predictive efficacy of the TyG index for massive IPN, and provide novel serological markers for the early clinical identification of vulnerable plaques.MethodsA total of 308 patients enrolled between May 2019 and December 2024 were included. IPN (0–3) was graded by Contrast-enhanced ultrasound (CEUS) and dichotomized (Grade I: none/minimal neovascularization, Grade II: extensive neovascularization). The association between the TyG and Grade II and its predictive performance were evaluated.ResultsThe proportion of IPN Grade II significantly increased with ascending TyG quartiles (Q1: 37.66% vs. Q4: 85.71%, P < 0.001). After adjusting for confounders, the risk of Grade II in the Q4 group was 7.32 times higher than in the Q1 group (95% CI: 2.81–19.05). Restricted cubic spline analysis revealed an exponential increase in risk when TyG > 8.28. Subgroup analysis demonstrated a stronger association between TyG and IPN Grade II in hypertensive populations. Furthermore, the TyG index yielded an area under the curve of 0.72, with a sensitivity of 81% and specificity of 60% at the optimal cutoff value of 8.645.ConclusionThis study demonstrates that the TyG index is significantly and independently associated with extensive IPN in carotid plaques. This finding suggests the TyG index has potential as a supplementary serological marker in the assessment of plaque vulnerability.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13098-025-01942-y.

BackgroundInflammation is a key driver of atherosclerosis, yet the mechanisms sustaining inflammation in human plaques remain poorly understood. This study uses a network-based approach to identify immune gene programs involved in the transition from low- to high-risk (rupture-prone) human atherosclerotic plaques.MethodsExpression data from human carotid artery plaques, both stable (low-risk, n = 16) and unstable (high-risk, n = 27), were analyzed using Weighted Gene Co-expression Network Analysis (WGCNA). Bayesian network inference, operated on the eigengene values from the WGCNA, further extended the WGCNA analysis, and similarity to the signature of T cell subsets was validated in single-cell RNA sequencing data of human plaques, and a loss-of-function study in a mouse model of atherosclerosis. In silico drug repurposing was performed to identify potential therapeutic targets.ResultsOur analysis revealed a distinct gene module with a prominent T cell signature, particularly in unstable plaques. Key regulatory factors, RUNX3, IRF7 and in particular PRDM1, were significantly downregulated in plaque T cells from symptomatic versus asymptomatic patients, indicating a protective role. Additionally, as PRDM1 is downstream of IRF7, we opted for PRDM1 as a key target. T cell-specific Prdm1 deficiency in Western-type diet fed Ldlr knockout mice featured accelerated plaque progression. Finally, as PRDM1 targeting drugs are not yet available, we performed in silico drug repurposing, identifying EGFR inhibitors as promising therapeutic candidates.ConclusionsThis study highlights a PRDM1-regulated T cell network that distinguishes high-risk from low-risk plaques and demonstrates the regulatory role of T cell PRDM1 in controlling atherosclerosis, positioning this pathway as a promising therapeutic target.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13073-025-01541-6.

The role of macrophage heterogeneity has become increasingly well-recognized in the study of vascular inflammatory responses. The CXCL4 (chemokine [C-X-C motif] ligand 4)-induced monocyte/macrophage phenotype has been implicated in atherosclerotic plaque destabilization, a key process preceding plaque rupture. Monocyte-derived macrophages differentiated with CXCL4 exhibit a unique transcriptome characterized by upregulation of S100A8 (S100 calcium-binding protein A8/calgranulin A) and MMP7 (matrix metalloproteinase-7). However, the mechanisms involved in CXCL4-induced monocyte-mediated vascular inflammation are unknown. Single-cell RNA sequencing data were examined for CXCL4-dependent transcriptional signatures in plaque macrophages. Human peripheral blood-derived monocytes (PBMCs) differentiated with CXCL4 were characterized in terms of osteogenic signatures and calcifying extracellular vesicle (EV) release. Association of the CXCL4-induced phenotype with the Wnt (wingless-type) pathway was investigated, and CXCL4-induced PBMC-derived EV were analyzed for their calcification potential in ECM (extracellular matrix) hydrogels and their ability to elicit an inflammatory response in vascular smooth muscle cells. In vitro findings were verified histologically in human carotid artery plaques. In human plaque macrophages, single-cell sequencing revealed a CXCL4-susceptible subpopulation bearing a distinct proinflammatory transcriptional signature. CXCL4-differentiated PBMCs exhibited a marked induction of S100A8, MMP7, and osteogenic marker transcription concomitant with augmented release of calcifying EV enriched with MMP7, S100A8, Anx5 (annexin 5), and ALP (alkaline phosphatase). Under osteogenic conditions, PBMCs and their secreted EV independently increased the calcification of the ECM in vitro. Analysis of inflammatory pathway activation identified the Wnt5a-CaMKII (wingless-type 5a-calcium/calmodulin-dependent protein kinase II) signaling axis to be linked to the CXCL4-induced osteogenic PBMC phenotype, EV calcification potential, and enrichment with MMP7 and S100A8. In addition, CXCL4-polarized PBMC-derived EV stimulated inflammatory gene expression in vascular smooth muscle cells. In human carotid artery plaques, CXCL4-induced macrophage abundance coincided with Wnt5a-CaMKII pathway activation and progressive plaque calcification. This study introduces a novel mechanism driving monocyte-mediated ECM remodeling in procalcific inflammatory responses through Wnt5a-CaMKII-activated secretion of MMP7+S100A8+ calcifying EV by CXCL4-induced proinflammatory monocytes.

An increased number of macrophages in the atherosclerotic plaque is associated with plaque instability and plaque progression. Lowering systemic cholesterol levels suppresses local macrophage proliferation and leads to plaque regression. However, the pathways regulating macrophage proliferation remain poorly understood. We investigated the cellular processes that underlie lipid-triggered local macrophage proliferation in the atherosclerotic plaque in transgenic mice and in human plaque tissue samples. Macrophages from mice with genetic deficiencies in scavenger receptors Cd36-/- and Msr1-/- showed reduced lipid uptake, lower intracellular lipid content, and lower proliferation compared to wild type macrophages. Double knockouts for the cholesterol exporters Abca1 and Abcg1 (MAC-ABC-DKO) showed increased rates of macrophage proliferation and apoptosis. In Cd36-/-, Msr1-/-, and MAC-ABC-DKO mixed bone marrow chimeras, no differences in chimerism were observed in blood or aorta after 4weeks on a high-cholesterol diet. After 12weeks of atherogenic diet, wild type macrophages predominated in the aorta since they proliferated more than neighboring Cd36-/- or Msr1-/- macrophages, and were less apoptotic than ABC-DKO macrophages, respectively. Knockout of NLRP3, but not ASC, Caspase 1 or IL-1 receptor, limited macrophage proliferation; indicating an NLRP3-dependent, but inflammasome-independent, effect. Inhibition of NLRP3 by MCC950 in human carotid artery plaque tissue cultures resulted in the suppression of intra-plaque macrophage proliferation and IL-1β release consistent with murine in vivo data. We identified a novel role for NLRP3 in driving macrophage proliferation in atherosclerotic plaques. NLRP3 inhibition may represent an ideal therapeutic target in atherosclerosis by combining anti-inflammasome and anti-proliferative effects in macrophages.

Objectives: While traditionally, carotid plaques with significant stenosis have been considered major embolic sources, recent evidence suggests that even non-stenotic small plaques with a <50% stenosis rate may contribute to cerebral infarction. Herein, we evaluated the relationship between non-stenotic small plaques and embolic stroke of undetermined source (ESUS) using computed tomography angiography (CTA). Materials and Methods: We retrospectively reviewed our single-institutional database of hospitalized patients with stroke between April 2017 and December 2022 and enrolled them with ESUS. We evaluated the presence or absence of non-stenotic carotid artery plaque lesions ipsilateral and contralateral to the cerebral infarction lesion using CTA. A neurologist, blinded to the stroke side and all other clinical information, reviewed each CTA and viewed the axial and sagittal CTA source images. In each image, a line perpendicular to the vessel wall was drawn and the plaque diameter was measured. The largest part was considered as the maximum plaque diameter. Results: A total of 951 patients with stroke were hospitalized during the study period. Among these, 35 patients with unilateral anterior circulation ESUS were enrolled. Plaque prevalence > 3 mm was compared between the carotid artery on the ESUS side and contralateral carotid artery. The prevalences were 31% and 8% on the ESUS and contralateral sides, respectively. Plaques > 3 mm were often found on the ESUS side. Conclusions: Patients with ESUS were more likely to exhibit non-stenotic plaques of ≥3 mm in the infarcted carotid artery than in the contralateral carotid artery. Thus, small non-stenotic plaques may be the embolization source in ESUS, and CT angiography is useful for these evaluations.

ObjectiveThis study evaluated therapeutic effects of ginsenoside Rg1 (QiShengli Tablets) in patients with carotid artery plaques, in combination with lifestyle interventions, lipid-lowering therapy. We aimed to provide novel insights into safe clinical application of ginsenoside Rg1 for managing cardiovascular and cerebrovascular diseases.MethodsFrom January 2022 to October 2023, 106 carotid artery plaques patients Aged ≥60 and <74 were recruited from the Geriatrics Department of First People’s Hospital of Yunnan Province. All participants provided informed consent and a randomized sequence is generated by random number table method and divided into three groups. Group 1 received lifestyle interventions plus atorvastatin calcium tablets (n = 32). Group 2 received same treatment as Group 1, with the addition of Bayaspirin (n = 33). Group 3 received the same treatment as Group 2, but with Bayaspirin replaced by ginsenoside Rg1 (n = 41). This study adopted a single-blind design: by uniformly encapsulating the tablets in their original form in blind bags, the subjects took them at regular intervals and in fixed quantities There were no significant differences in baseline characteristics among the groups before treatment (P > 0.05). All patients were treated 3 months. Carotid atherosclerosis–related outcomes were assessed after treatment, and data were analyzed using SPSS 24.0.ResultsCarotid ultrasound revealed significant intergroup differences in plaque number and volume changes after treatment (P < 0.05). No significant intergroup differences were observed in arterial stiffness index (P > 0.05). Fibroblast growth factor 21 levels differed significantly among the groups (P < 0.05), whereas Lumican and Fibulin-1 levels did not (P > 0.05). Analysis biochemical indicators revealed significant post-treatment differences in LDL-C, TC, Hcy, IL-6, TNF-α, 25(OH)D, and insulin resistance (IR) (P < 0.05). Notably, after treatment of three groups, Montreal Cognitive Assessment (MoCA) scale score was statistically significant (P < 0.05).ConclusionPatients with carotid atherosclerotic plaques, adding ginsenoside Rg1 to standard therapy reduced the number and volume of carotid plaques. It improved quality of life, decreased specific inflammatory markers, and enhanced blood pressure control and Insulin Resistance (IR). These suggest ginsenoside Rg1 may have clinical value in the future management of carotid atherosclerosis.

Correlation between serum uric acid and carotid artery plaque in ischaemic stroke patients based on age, blood pressure condition, and sex stratification.

Atherosclerosis progresses after starting renal replacement therapy, and it contributes to high cardiovascular mortality. Carotid intima-media thickness (CIMT) and plaque offer a convenient method to explore the status of systemic atherosclerosis. The aim of this cohort study was to determine the significance of carotid plaque and other factors that may impact the clinical outcomes of end-stage renal disease (ESRD) patients. Two hundred and sixty-five patients who received maintenance hemodialysis for more than 3 months were enrolled in the study and closely followed for 2 years with clinical events recorded. The primary endpoint was cardiovascular death. During the 2-year follow-up period, 11.7% of the patients died from cardiovascular causes; however none were caused by stroke. The patients with carotid plaques were older and had thicker left CIMT and right CIMT, lower serum albumin, higher alanine aminotransferase, higher serum glucose, lower serum creatinine, and higher rates of cardiovascular death and overall mortality. Logistic regression analysis showed that the existence of carotid plaque (odds ratio 3.39, 95% confidence interval: 1.577-7.292, p = 0.002) was significantly correlated with the primary outcome. Plaque also significantly impacted overall survival (log-rank p = 0.024). The presence of carotid plaque was a risk factor for cardiovascular death in patients with ESRD.

Prevalence of carotid atherosclerosis in 3-92-year-old Finns. The 3-generational cardiovascular risk in young Finns study.

Emerging cytokines contribute to the clinical manifestation of carotid artery plaque formation and stability in patients with diabetes.

Objective: To investigate the correlation between plasma inflammatory biomarkers MMP-9, Lp-PLA2, IL-6, TNF-α and vascular cognitive impairment in patients with cerebral small vessel disease (CSVD), and to provide theoretical evidence for the early diagnosis and treatment of cognitive impairment in patients with cerebral small vessel disease. Methods: A total of 400 patients admitted to the Department of Neurology, Xuzhou Central Hospital, for treatment of CSVD from January 2019 to June 2023 were randomly selected. The cognitive function of the patients was assessed using the Montreal Cognitive Assessment (MoCA) scale. Based on the scores, the patients with CSVD were divided into a normal cognition group (n=196) and a cognitive impairment group (n=204). According to the severity of cognitive impairment, the cognitive impairment group was further divided into mild cognitive impairment group (n=100), moderate cognitive impairment group (n=59),and severe cognitive impairment group (n=45). A healthy control group of 100 individuals who underwent physical examinations during the same period was included. The correlation between plasma inflammatory biomarkers MMP-9, Lp-PLA2, IL- 6, TNF-α and vascular cognitive impairment was studied. Results: Compared with the healthy control group, the levels of smoking, homocysteine (HCY), carotid artery plaque formation, MMP-9, Lp-PLA2, IL-6, TNF-α in the normal cognition group and cognitive impairment group of patients with CSVD were significantly increased, with statistical significance (P&lt;0.05). Moreover, the levels of smoking, HCY, carotid artery plaque formation, MMP-9, Lp-PLA2, IL-6, TNF-α in the cognitive impairment group were higher than those in the normal cognition group, with statistical significance (P&lt;0.05). Multivariate logistic regression analysis showed that after controlling for confounding factors such as smoking, HCY, and carotid artery plaque formation, MMP-9, Lp-PLA2, IL-6, and TNF-α in patients with CSVD were still positively correlated with vascular cognitive impairment (P&lt;0.05) and were independent risk factors. Compared with the mild cognitive impairment group, the levels of plasma MMP-9, Lp-PLA2, IL-6, and TNF-α in patients with moderate and severe cognitive impairment were significantly increased, with statistical significance (P&lt;0.05); compared with the moderate cognitive impairment group, the levels of plasma MMP-9, Lp-PLA2, IL-6, and TNF-α in patients with severe cognitive impairment were significantly increased, with statistical significance (P&lt;0.05). There was a negative linear relationship between plasma inflammatory biomarkers MMP-9, Lp-PLA2, IL-6, and TNF-α levels and cognitive function scores (P&lt;0.05). Conclusion: Plasma MMP-9, Lp-PLA2, IL-6, and TNF-α are independent risk factors for vascular cognitive impairment in patients with CSVD. Plasma MMP-9, Lp-PLA2, IL-6, and TNF-α levels in patients with CSVD are positively correlated with the severity of vascular cognitive impairment.

The illicit use of anabolic androgenic steroids (AAS) is common among recreational athletes, yet studies on adverse cardiovascular outcomes, especially in female AAS users, are sparse. To assess cardiovascular status in Danish male and female recreational athletes using AAS compared with not using AAS. This cross-sectional study in a single center in Denmark included recreational athletes aged 18 years or older who were active AAS users, previous users (defined as those who discontinued AAS use at least 3 months prior to the study), or nonusers, all recruited from fitness centers between March and December 2022. Cumulative lifetime use of AAS. Presence of atherosclerosis (carotid, femoral, and coronary artery plaques) and cardiac function assessed by echocardiography. Linear regression was used to estimate regression coefficients for echocardiographic characteristics and logistic regression to estimate odds ratios (ORs) for carotid and femoral plaques, coronary artery calcium (CAC) scores, and coronary noncalcified plaques (NCPs). Of 164 participants, 80 (48.8%) were active AAS users (median age, 35 [IQR, 30-43] years; 61 men [76.2%]), 26 (15.9%) were previous users (median age, 36 [IQR, 28-51] years; 18 men [69.2%]), and 58 (35.4%) were nonusers (median age, 40 [IQR, 31-46] years; 42 men [72.4%]). Median cumulative lifetime AAS use was 2.2 (IQR, 1.2-7.2) years for active and 2.2 (IQR, 1.0-5.5) years for previous users. No group differences were observed when comparing the number of participants with femoral (active users, 15 [19.7%]; previous users, 5 [19.2%]; nonusers, 11 [20.8%]; P = .89) or carotid (active users, 24 [31.2%]; previous users, 12 [46.2%]; nonusers, 13 [24.1%]; P = .47) artery plaques or CAC scores (median score was 0 across all groups with range of 0-228 for active users, 0-800 for previous users, and 0-163 for nonusers; P = .36), whereas a statistically significant difference in the prevalence of coronary NCPs was found between active users (19 [23.8%]) and nonusers (6 [10.3%]) (P = .03). However, in confounder-adjusted logistic regression, longer cumulative lifetime AAS use was associated with higher odds of a positive CAC score (OR, 1.23; 95% CI, 1.09-1.39; P = .001) and presence of coronary NCPs (OR, 1.17; 95% CI, 1.05-1.30; P = .004). AAS use exceeding 5 years was associated with greater severity of calcifications (n = 94; χ2 = 9.78; P = .04). Echocardiography showed that cumulative AAS use was associated with worse left ventricular (regression coefficient: 0.08; 95% CI, 0.03-0.12; P = .002) and right ventricular (0.08; 95% CI, 0.03-0.13; P = .001) global longitudinal strain. Nearly all athletes (35 of 36) with more than 5 years of cumulative AAS use had ventricular mass greater than and left ventricular ejection fraction below the median of the normal range. In this cross-sectional study, cumulative lifetime AAS exposure was associated with adverse cardiovascular findings and impaired ventricular function in both sexes, and athletes with AAS exposure exceeding 5 years showed more severe calcification. The findings support measures to prevent AAS use by both men and women in recreational sports.

ObjectiveThis study aims to differentiate between symptomatic and asymptomatic plaques using a computed tomography angiography (CTA)-based radiomics model of perivascular adipose tissue (PVAT).MethodsPatients were categorized into symptomatic and asymptomatic groups based on the presence or absence of acute ischemic stroke or transient ischemic attack in the anterior cerebral circulation within two weeks prior to the CTA examination. The clinical information of all patients was collected and analyzed, and the PVAT features of CTA images were further analyzed to clarify their correlation with plaque classification. K-nearest neighbors (KNN), support vector machine (SVM), logistic regression (LR), random forest (RF), linear discriminant analysis (LDA), multinomial naive Bayes (MultinomialNB), and extreme gradient boosting (XGBoost) were trained and radiomics (Rad) score was calculated using the best classifier. A combined model was further developed based on the Rad-score and independent predictors, and the calibration, receiver operating characteristic curve, decision curve analysis, and clinical applicability were evaluated.ResultsThe white blood cell count and hyperlipidemia were clinically independent predictors, and ten PVAT radiomics features showed significant correlation. The XGBoost classifier showed the best performance among different classifiers, with an average AUC of 0.797 in the validation set. The combined model integrating Rad-score and clinically independent predictors was further obtained, with AUCs of 0.942, 0.797, and 0.836 in the training, external validation sets, respectively.ConclusionThe combined model performed excellently in predicting symptomatic carotid plaques. By early identification of high-risk patients and selecting appropriate clinical decisions, it holds significant clinical potential for improving stroke prevention.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12880-025-01876-x.

BackgroundThis study aimed to investigate the prospective association of dairy biomarkers of odd-chain saturated fatty acids (OCFA) with incident carotid artery plaque (CAP) and to explore the potential role of gut microbiota and related metabolites in the above associations.MethodsIn the Guangzhou Nutrition and Health Study (GNHS, n = 1211; baseline mean age: 58.7 ± 6.1 years), we investigated the associations of baseline plasma phospholipid OCFAs with CAP incidence and gut microbiota (16S rRNA sequencing) over a median follow-up period of 6.2 years. Westlake Precision Birth Cohort was used to evaluate the potential associations between OCFA and the identified gut microbiota features in a younger population. Associations of OCFAs with CAP, gut microbial alpha diversity, specific genera, and related metabolites were examined using Cox proportional hazards models or linear regression models, with adjustments of potential confounders.ResultsThe total OCFA was inversely associated with the incidence of CAP in the GNHS, with a hazard ratio of 0.63 (quartile 4 versus 1: 95% confidence interval [CI]: 0.46, 0.86). Additionally, total OCFA was significantly associated with gut microbial alpha and beta diversity (all P < 0.05). The beta coefficient for the association between total OCFA and the Shannon index was 0.11 (95% CI: 0.06, 0.17). We identified 36 microbial genera significantly associated with total or individual OCFAs (FDR < 0.05). Among these identified genera, the Christensenellaceae R-7 group, an OCFA-positive-related genus, was inversely associated with the prevalence of CAP (P < 0.05). We then identified 13 microbe-derived metabolites significantly associated with both total OCFA and C. R-7 group (FDR < 0.05), including deoxycholic acid and lithocholic acid.ConclusionsOur results suggest that plasma OCFAs, as objective biomarkers of dairy exposure, are inversely associated with CAP incidence in a Chinese cohort. Further exploration indicates that gut microbiota may be involved in the above association, providing a potential gut microbiota-based intervention target for atherosclerosis.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12916-025-04307-4.